Expression profile of human breast cancer cells with CEBPB overexpression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Pei Yi Xia
PROVIDER: E-GEOD-67425 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2015-02-11 | E-GEOD-65801 | biostudies-arrayexpress
Project description:To further verify the underlying functions of Bit1 in ESCC, therefore, in the present study, we examined Bit1 expression in a panel of ESCC cell lines, and investigated the effects of Bit1 knockdown on tumor growth, migration and invasion as well as cell apoptosis in ESCC, and further preliminarily elucidated the possible molecular mechanisms. All data presented herein suggest Bit1 may be a promising molecular target for the therapy of ESCC, and thus intervention of Bit1 may lead to better therapeutic outcomes for the patients with ESCC. To further verify the underlying functions of Bit1 in ESCC, therefore, in the present study, we examined Bit1 expression in a panel of ESCC cell lines, and investigated the effects of Bit1 knockdown on tumor growth, migration and invasion as well as cell apoptosis in ESCC, and further preliminarily elucidated the possible molecular mechanisms. All data presented herein suggest Bit1 may be a promising molecular target for the therapy of ESCC, and thus intervention of Bit1 may lead to better therapeutic outcomes for the patients with ESCC. EC9706 cells were harvested 72 h after transfection with pSilencer3.1-H1 -neo-Bit1-shRNA or pSilencer3.1-H1-neo-negative-shRNA. Approximate 1â??Ã?â??106 cells from each sample were subjected to gene microarray assay. Total RNA was extracted was extracted for analysis.
2016-03-03 | E-GEOD-78813 | biostudies-arrayexpress
Project description:To explore the molecular mechanisms and signal pathways induced by restoring tumor suppressor gene HIC-1 on breast cancer cells. We have employed whole genome microarray expression profiling as a discovery platform to identify the differential genes induced by HIC-1 gene activation. Small activating RNA (saRNA) that targeted promoter region was used, and MCF-7 breast cancer cell line was selected as cell model. After 96h for saRNA transfection, the cells were collected and the whole genome expression profiles were analyzed. Three independent experiments were repeated for different groups. With the treshold of p<0.01 and fold change >=2 or <-2, there were 1375 differential expression genes, which are related to cell cycle, apoptosis, cell migration, cell invasion and cell proliferation. SaRNA induced gene expression in human breast cancer cell MCF-7 was measured at 96 hours after transfection by 50 nM saRNA. Three independent experiments were performed for experimental group and control group.
2012-11-06 | E-GEOD-42024 | biostudies-arrayexpress
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Project description:Purpose: We aimed to investigate the effect of several anti-leukemia drugs in combination with decitabine (DAC) on the proliferation of myeloid leukemia cells in vitro and in vivo, to select the most efficient combination group and explore associated mechanisms of these combination therapies. Experimental Design: After comparing with five anti-leukemia drugs in several different kinds of cell lines, the combination effect of idarubicin (IDA) with DAC was best. In vivo, by using microPET, TUNEL, and transmission electron microscopy, the inhibitory effects obtained by sequentially combining DAC with IDA, evidenced by evaluating tumor cell proliferation and cell apoptosis. Molecular studies were conducted using gene chip, which was used to explore associated pathways, and real-time quantitative reverse transcription-PCR, western blot and immunohistochemistry (IHC), used to assess regulation of Wnt/β-catenin pathway. Results: The sequential combination of DAC and IDA showed synergistic induction of cell death in U937, HEL, SKM-1 and cells isolated from AML patients. Importantly, the inhibition of tumor growth in the sequential combination group was found to be significantly higher than that of single drug group or control group in vivo. Moreover, sequential treatment with DAC and IDA induced apoptosis and depression of the Wnt/β-catenin pathway in both culture and animal studies. Conclusions: Our findings showed that sequentially combining decitabine with idarubicin had a synergistic anti-leukemia effect. These findings were attributed to demethylation of Wnt pathway inhibitors and downregulation of Wnt pathway nuclear targets observed in vitro and in vivo. After comparing with five anti-leukemia drugs in several different kinds of cell lines, the combination effect of idarubicin (IDA) with DAC was best. In vivo, by using microPET, TUNEL, and transmission electron microscopy, the inhibitory effects obtained by sequentially combining DAC with IDA, evidenced by evaluating tumor cell proliferation and cell apoptosis. Molecular studies were conducted using gene chip, which was used to explore associated pathways, and real-time quantitative reverse transcription-PCR, western blot and immunohistochemistry (IHC), used to assess regulation of Wnt/β-catenin pathway.
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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